Consultant on Call CARDIOLOGY

Peer Reviewed Adrian Boswood, MA, VetMB, MRCVS, DVC,

Diplomate ECVIM (Cardiology)
University of London

Chronic Valvular Disease in the Dog

PROFILE also likely to develop the disease when young.3
● It is currently unclear whether CVD is herita- Since CVD is such a
Definition ble in other breeds and to what extent inheri- common cause of
● Chronic valvular disease (CVD) is the most tance influences disease development acquired heart dis-
common cardiovascular disease in small compared to other factors. ease in dogs, any
animals.1 CVD is estimated to cause approxi- ● Males appear to develop the disease at an older small-breed
mately 75% of canine cardiac disease encoun- earlier age.4 dog with a typical
tered in practice. murmur should be
• The cardiac valve most commonly affected is Pathophysiology suspected of having
the mitral valve, and CVD is also known as ● CVD is characterized by loss of normal
the condition.
degenerative mitral valve disease, myxomatous integrity of the valve, with disruption and
mitral valve disease, and endocardiosis. weakening of normal valvular structures.
● The principal hemodynamic abnormality that
Signalment results from valvular changes is mitral regurgi-
Age & Range tation. This introduces a functional ineffi-
● CVD usually affects older small-breed dogs, ciency to the left side of the heart.
although some larger breeds can develop the ● To ensure sufficient blood flow out of the left
condition.2 ventricle into the systemic arterial circulation,
● The disease course in larger dogs is often the ventricle must pump a greater than normal
slightly different; this article will focus on typ- volume of blood to compensate for the volume
ical presentation and progression of CVD in being ejected, in a retrograde manner, into the
small-breed dogs. left atrium (regurgitant stroke volume).
● Over time, the valvular changes progress, lead-
Breed & Sex Predilection ing to larger regurgitant volume and progres-
● Evidence suggests that CVD is a heritable sively greater compensatory effort by the heart
trait in some breeds. For example, in the and circulatory system.
Cavalier King Charles spaniel, the offspring of
parents affected by CVD at a younger age are CVD = chronic valvular disease CONTINUES

Consultant on Call / NAVC Clinician’s Brief / December 2010...............................................................................................................................................................17

 Consultant on Call CONTINUED

DEFINITIONS Clinical Signs low intensity, left-sided systolic heart murmur.

● Left-sided heart ● In early stages of CVD, when regurgitant vol- The murmur is typically most audible at the
failure: Fluid accumu- ume is low, the patient is usually able to com- left heart apex where the impulse of the car-
lation in the lungs pensate easily and often demonstrates no diac contraction is most palpable. (For addi-
● Mitral regurgitation: clinical signs. This phase can last several years. tional information on left-sided heart
Blood regurgitates ● As the valve leak worsens, clinical signs may murmurs, see the Table.)
through the mitral valve become evident (see Clinical Signs of CVD); ● As the murmur becomes louder due to disease
from the left ventricle in addition, signs of congestion may develop progression, it may radiate and become audible
into the left atrium dur- secondary to excessive fluid retention (precipi- over other areas of the thorax (typically dor-
ing cardiac contraction tated by the neuroendocrine response to heart sally and to the right).
● Right-sided heart disease). ● Signs of more advanced disease (and of patients’
failure: Fluid ● It is estimated that < 25% of affected dogs efforts to compensate for their disease) include
accumulation in develop signs associated with CVD; many elevated heart rate (> 140 beats/min), loud
the systemic veins and develop and succumb to other diseases of heart murmur, and loss of respiratory sinus
body cavities. aging dogs. arrhythmia.
● In patients with sufficiently advanced disease,
Physical Examination there may be other abnormalities, including:
● In patients being examined annually (or more ◗ Pulmonary crackles indicating pulmonary
frequently), CVD is usually indicated initially edema (patients with left-sided heart failure)
by discovery of a heart murmur in an other- ◗ Ascites and jugular venous distension
CLINICAL SIGNS
wise healthy dog. In patients examined less (patients with right-sided heart failure)
OF CVD
frequently, onset of signs noted by the owner ◗ Irregular cardiac rhythm and pulse deficits
may be the first indication. (patients with arrhythmias)
When the heart can no
longer meet the demands ● The most characteristic finding in dogs with
of metabolically active mitral regurgitation secondary to CVD is a
tissues, clinical signs of
CVD may result.
● Dyspnea (left- and
right-sided heart Table. Differential Diagnosis of a Left-Sided Heart Murmur
failure)*
● Cough Cause of Murmur Relevant Considerations
● Exercise intolerance Aortic stenosis* Murmur usually more audible at left heart base
● Syncope or episodic
Atrial septal defect* Murmur most audible at pulmonic valve (ie, left heart base)
weakness
and usually of very low intensity
● Lethargy
● Nocturnal restlessness Mitral regurgitation Most frequently caused by CVD but may be secondary to
● Ascites (right-sided other causes, including congenital dysplasia, ventricular
heart failure)* dilatation due to dilated cardiomyopathy, and bacterial endo-
carditis
● Pallor
● Hypotension Patent ductus arteriosus* Murmur is most intense in systole and usually continuous
● Unexplained weight and audible with a point of maximal intensity dorsal and
loss cranial on the thoracic wall
Pulmonic stenosis* Murmur more audible at left heart base
* Signs of congestion second-
ary to excessive fluid reten- Ventricular septal defect* Murmur sometimes most audible on the left, but typically has
tion point of maximal intensity on right side of thorax
* Condition usually congenital in origin; therefore, more likely found in young animal

CVD = chronic valvular disease

18...............................................................................................................................................................NAVC Clinician’s Brief / December 2010 / Consultant on Call

 Color Doppler echocardiographic image (obtained from right side of the thorax)
of a patient with marked mitral regurgitation: The heart is seen in long axis
with the left ventricle displayed on the left side of the image and left atrium to
the right. Mitral regurgitation is indicated by presence of a large, vividly colored
jet of blood regurgitating from the left ventricle into the left atrium during ven-

1
tricular systole.

DIAGNOSIS

There are 4 critical questions that need to be

answered to develop a management plan for
patients with CVD:
● Is the disease definitely CVD?
● Is cardiomegaly present?
● Is evidence of heart failure present?
● Does the patient have evidence of concurrent
disease?

Definitive Diagnosis
Echocardiography
● Definitive diagnosis is made by identifying a
distorted mitral valve and evidence of valvular
insufficiency (in the absence of other cardiac
disease); this can be achieved using echocar- Additional Diagnostics
diography and Doppler echocardiography Radiography
(Figure 1), respectively. ● The optimal monitoring test for dogs with
● Clients may decide not to pursue Doppler
CVD is thoracic radiography (Figure 2). This
echocardiography, particularly if their pets are can be undertaken at regular intervals (eg,
not showing outward signs. annually) to document evidence of progressive
● If the course of CVD in a small-breed dog is
enlargement of the cardiac silhouette.
typical, many times a clinical diagnosis is made ● Thoracic radiography is regarded as the best
without definitive confirmation; however, if diagnostic test for diagnosing left-sided heart
clients pursue optimal management, including failure (indicated by pulmonary venous con-
definitive confirmation, Doppler echocardiog- gestion and pulmonary edema).
raphy should be recommended to ensure an
CONTINUES
accurate diagnosis.

A B
2
Radiographs of the same patient taken over
5 years depicting the gradual progression of
cardiomegaly secondary to valvular heart dis-
ease typically found in CVD patients. In D,
which shows marked cardiomegaly and left
atrial enlargement, left-sided heart failure is
indicated by presence of increased alveolar-
interstitial density within the lung field.

C D

Consultant on Call / NAVC Clinician’s Brief / December 2010..............................................................................................................................................................19

 Consultant on Call CONTINUED

Electrocardiography Significant Cardiomegaly But No Clinical

MORE
For further information,
see Cardiac N-Terminal
Pro–B-Type Natriuretic
Peptide Assay (July
2010) by Dr. Mark Oyama,
available at clinicians
brief.com/journal.
ACE = angiotensin-converting
enzyme; CVD = chronic valvular
disease; NT-proBNP = N-termi-
nal pro–B-type natriuretic pep-
tide
● Electrocardiography is useful in patients Signs
suspected of having a cardiac arrhythmia. ● Treatment at this stage remains controversial:
● It has limited value in identifying cardio- some cardiologists advocate therapy in an
megaly and almost no value in diagnosis of effort to prevent signs of heart failure; others
heart failure. do not initiate treatment until signs have
developed. (The author falls into the latter
Laboratory Analysis group.)
● Routine hematology and biochemical profiles ● Two prospective double-blinded, placebo-con-
are rarely useful for diagnosing CVD but can trolled studies examined the hypothesis that
rule out other potential diseases (eg, bacterial angiotensin-converting enzyme (ACE)
endocarditis). inhibitors would slow the development of
● Serum biochemical profiles can also determine heart failure.5,6 Neither study convincingly
whether any renal or hepatic disease, which demonstrated a significant difference in the
could complicate management of cardiac dis- time to their primary endpoint.
ease, is present.
Cardiomegaly & Clinical Signs
NT-proBNP Assessment ● Once signs of congestive heart failure have
● Cardiac N-terminal pro–B-type natriuretic developed, therapy can result in improvement
peptide (NT-proBNP) is a blood-based assay of clinical signs and use of certain agents
that can help detect underlying heart disease. results in improved survival.7,8
● Levels of this peptide increase in plasma as ● Furosemide & pimobendan: Following publi-
the severity of valvular heart disease increases. cation of the QUEST study8 it appears opti-
In essence, higher concentrations are likely to mal chronic management of patients with
indicate more advanced disease. mitral regurgitation should include adminis-
tration of these medications.
TREATMENT ● ACE Inhibitors: It is widely believed by cardi-
ologists that ACE inhibitors provide addi-
Patients with CVD can be divided into 3 treat- tional benefits, although this is not a
ment groups: conclusion that can be drawn from the
● Dogs without cardiac enlargement and clinical QUEST study due to its design.
signs ● Spironolactone: There is also some evidence
● Dogs with significant cardiomegaly but no that spironolactone administration may help
clinical signs control signs of heart failure and possibly pro-
● Dogs with cardiomegaly and clinical signs, long survival.
especially signs of congestive heart failure ● Whether all 4 drugs should be introduced at
once or some reserved for use once dogs have
No Cardiac Enlargement or Clinical Signs become refractory to initial therapy is often a
● Optimal management at this stage consists of matter of a cardiologist’s personal preference and
client education, including instruction regard- influenced by owner finances and issues of
ing optimizing weight, regular exercise, and compliance.
identifying signs that may indicate progression ● In cases with acute onset of severe heart failure,
of CVD. emergency therapy with intravenous diuretics,
● Over-emphasizing the potential severity of oxygen supplementation, other vasodilators, and
CVD may cause undue anxiety for owners. It inotropic agents may be necessary.
is important to stress that many patients have
a relatively benign course and will never go on
to develop signs.

20...............................................................................................................................................................NAVC Clinician’s Brief / December 2010 / Consultant on Call

Heart Failure Refractory to Therapy cator of resolution of pulmonary congestion
● Many agents have been advocated for use in and edema. Auscultation Tip
dogs developing persistent signs of heart fail-
ure refractory to initial management, includ- Adverse Reaction to Medications In order to decide if a
ing: ● Many drugs administered to patients with murmur is basilar or
◗ Additional diuretics (thiazides, spironolac- heart failure secondary to CVD act on, or are apical on the left sys-
tematically move the
tone, torsemide) excreted by, the kidneys. They may induce stethoscope forward
◗ Additional vasodilators (hydralazine, azotemia and electrolyte disturbances.11 and back on the left
amlodipine) ● The best way to monitor for adverse reactions side of the thorax dur-
◗ Digoxin is to perform a limited serum biochemical pro- ing auscultation. If the
● At this stage, therapy is empirical; there is file that includes urea, creatinine, sodium, and murmur becomes less
audible as the stetho-
little evidence to support one method of treat- potassium approximately 7 days after therapy scope is moved cra-
ment over another. initiation and after any change in therapy. nially and louder as the
stethoscope is moved
Chronic Cough Secondary to CVD Monitoring at Home caudally over the area
● Cough is frequently not a consequence of ● As mentioned previously, improvements in of the heart, the mur-
mur is probably apical.
congestion but a result of increased heart size, respiratory rate and effort are good indicators
compression of adjacent structures, and possi- of successful therapy and can be monitored at
ble bronchial collapse in certain breeds of home.
dogs. ● Attentive owners can also detect evidence of
● In this circumstance, agents, such as broncho- deterioration, particularly if respiratory rate is
dilators, cough suppressants, and intermittent observed and recorded at regular intervals.
antiinflammatory medication, may need to be
considered. IN GENERAL

Nutritional Aspects Prognosis

● Diets have been shown to modify some indica-
tors of disease,9 such as heart size and concen-
trations of neurohormones, but this has yet to
translate into demonstrable improvement in
outcome.
● Of the various supplements described for use
in CVD, evidence is probably most compelling
for use of omega-3 fatty acids.10 However, sur-
vival benefit in dogs is currently lacking.
● The main advice I offer with respect to diet is
to maintain a healthy weight and aim for
modest, consistent levels of sodium intake.
FOLLOW-UP
Monitoring Therapy Success
● Success of therapy is determined by resolution
of signs of heart failure. If radiographic
evidence of heart failure was a reason for initi-
ating therapy, thoracic radiographs should be
repeated.
● Reduction in respiratory rate and effort in
hospitalized patients is also a very good indi-
● Early CVD can be regarded as a fairly benign
disease; it is likely that as few as 25% of dogs
with CVD will succumb to this disease.
● Animals with clinical signs of heart failure
tend to have progressive cardiomegaly prior to
development of signs.
● Even with optimal therapy, 50% of dogs with
heart failure will die within the first 6 to 12
months.8,12
Future Considerations
In human patients, the optimal method of man-
aging valvular heart disease is surgical replace-
ment or repair of the valve.13,14 Although limited
case reports have described similar techniques in
dogs, it is likely that cost and limited access to the
technique will mean this remains an uncommon
method of managing CVD.
See Aids & Resources,
back page, for references
& suggested reading.

Consultant on Call / NAVC Clinician’s Brief / December 2010...............................................................................................................................................................21